The ionic basis of nerve cell excitability and the actions of ethanol on those mechanisms were investigated using electrophysiological methods. Sodium and calcium currents were characterized in adult mammalian neurons acutely isolated from rat nodose ganglion using the whole cell patch-clamp method. Two types of sodium current were observed. One current was abolished by 3-15 micromolar tetrodotoxin (TTX), had a rapid time course, activated over the potential range -70 to -10 mV, and attained half-maximal conductance at -30 mV. The other current persisted in the presence of 15 micromolar TTX, had a slower time course, activated over the potential range -30 to 0 mV, and attained half-maximal conductance at -10 mV. Two calcium current components were observed in some cells, an inactivating component that activated near -60 mV, and a large sustained current that activated near -40 mV. The results indicate that some cells have more than one type of sodium and/or calcium channel. Calcium current was also studied in CA3 pyramidal neurons in hippocampal slice using the single-electrode voltage clamp. The calcium current activated rapidly and gradually decayed with maintained depolarization. Upon return to a more hyperpolarized potential, the calcium current decayed with both a rapid and a slow component. The rapid component was too fast to be followed by the single-electrode clamp. The decay of the slow component could be described by a single exponential function that was dependent upon the potential of the neuron. The decay time course suggests that there are two or more types of calcium channels in these central neurons. The effect of ethanol is being tested on these ion currents. The significance of the project lies in the fact that the identification of the mechanisms involved in nerve cell excitability and the action of ethanol on those mechanisms hold the promise of increasing our understanding of the cellular basis of ethanol's actions in the nervous system.